Lactobacillus acidophilus is a Gram-positive, rod-shaped, non-spore forming, homofermentative bacterium that is a normal inhabitant of the gastrointestinal and genitourinary tracts. Since its original isolation by Moro (1900) from infant feces, the “acid loving” organism has been found in the intestinal tract of humans, breast fed infants, and persons consuming high milk-, lactose-, or dextrin diets. Historically, Lactobacillus Acidophilus is the Lactobacillus species most often implicated as an intestinal probiotic capable of eliciting beneficial effects on the microflora of the gastrointestinal tract (Klaenhammer and Russell (2000) “Species of the Lactobacillus acidophilus Complex,” in Encyclopedia of Food Microbiology, Volume 2, ed. Robinson et al., (Academic Press, San Diego, Calif.), pp. 1151-1157). Lactobacillus Acidophilus can ferment hexoses, including lactose and more complex oligosaccharides (Kaplan and Hutkins (2000) Appl. Environ. Microbiol. 66:2682-2684) to produce lactic acid and lower the pH of the environment where the organism is cultured. Acidified environments (e.g. food, vagina, and regions within the gastrointestinal tract) can interfere with the growth of undesirable bacteria, pathogens, and yeasts. The organism is well known for its acid tolerance, survival in cultured dairy products, and viability during passage through the stomach and gastrointestinal tract. Lactobacilli and other commensal bacteria, some of which are considered as probiotic bacteria that “favor life,” have been studied extensively for their effects on human health, particularly in the prevention or treatment of enteric infections, diarrheal disease, prevention of cancer, and stimulation of the immune system.
Microbial esterases and lipases are presently of interest because of their potential applications in biotechnology for food processing, surfactant composition, detergents, paper, oil manufacture, diagnostics, and optically active drugs (Jaeger et al. (1999) Annu. Rev. Microbiol. 53:315-351, Jaeger and Reetz (1998) Trends Biotech. 16:396-403). The enzymes that modify milk fat are lipases (triacylglycerol lipases; EC 3.1.1.3) and esterases (EC 3.1.1.1). Esterases are, by definition, enzymes that have the ability to hydrolyze ester substrates with short-chain fatty esters (≦C10), whereas lipases hydrolyze long-chain acylglycerols (≧C10) (Verger (1997) Trends Biotech. 15:32-38). The substrates and products of these enzymes may be involved in the formation of various flavor components of maturing cheeses, fermented dairy products, cured bacon and fermented sausages. It has been an interest in the dairy field to reduce the inherent cost and to enhance flavor intensity of various cheeses by shortening the maturation period in their preparation and processing. The free fatty acids, which are liberated by the action of lipases or esterases on milk fat, give dairy products their typical flavor characteristics. Upon further breakdown of fatty acids, reactions with other components of maturing cheeses and fermented dairy products, which may contribute to the formation of various flavor components, are likely to occur (Stead (1986) J. Dairy Sci. 53:481-505).
Oxalic acid is a strong dicarboxylic acid (pKa1=1.23; pKa2=3.83) and a toxic compound that irritates tissues. This effect was recognized in the eighteenth century, when used for cleaning and bleaching. Oxalate in extremely high concentrations can cause death in humans and animals, and pathological disorders, including hyperoxaluria (an oxalate level exceeding the normal range), pyridoxine deficiency, urolithiasis (formation of calculi or uroliths), renal failure, and others (Hatch et al. (1995) Scanning Microsc 9:1121-1126). The toxicity of oxalate has been related to its capability to generate reactive oxygen species (through the Fenton reaction) as hydroxyl or carbonate radicals during its interaction with hydrogen peroxide (Park et al. (1997) Free Rad Res 27:447-458 and Urzua et al. (1998) Appl. Envirn. Microbiol. 64:68-73). Oxalate occurs widely in nature and many foods such as boiled carrots (1.88 mg/g), tomatoes (0.04 mg/g), celery (0.17 mg/g), potato (0.02 mg/g) and corn (0.03 mg/g), and other dietary sources such as tea (0.11 mg/ml), coffee (0.05 mg/ml) and chocolate (1.17 mg/g). Oxalic acid can also be produced by non enzymatic degradation or from some metabolic precursors (like ascorbic acid) by the intestinal microflora (Ogawa et al. (2000) World J. Surg. 24:1154-1159). In the intestine, oxalate may combine with calcium, sodium, magnesium, or potassium forming less soluble salts, but also with iron generating high soluble salts. The presence of bacteria that specifically degrade oxalate has been proposed to regulate the oxalate homeostasis of the host by preventing absorption, catabolizing free oxalate and enhancing oxalate secretion from the circulation. A recent clinical study has demonstrated a correlation between low rates of intestine colonization with oxalate-degrading bacteria, specifically Oxalobacter formigenes, with an increased risk of hyperoxaluria due to an increase in urinary oxalate concentration (Troxel et al. (2003) J. Endourol. 17:173-176). Accordingly, compositions and methods are needed in the art that can modulate oxalate degradation.